The control of undesirable plants by the use of herbicides is an extensively used practice and the market for herbicidal compounds continues to expand. However, some weedy plant species are resistant to some of these herbicidal compounds. As a result, either greater amounts of the herbicidal compounds must be applied to control these weeds, or herbicides with greater potency have to be used. The result in either case can frequently be a sensitivity of desirable crop plants to the herbicidal compounds. An alternative to the use of increased amounts of herbicides or the application or identification and development of new herbicides for use with particular crop plants is the modification of susceptible or sensitive crop species so that they are resistant or tolerant to specific herbicides. This strategy of modifying susceptible or sensitive crop species should reduce chemical herbicide input while at the same time maximizing weed control. A number of methods exist for achieving this goal, and one such method is through the genetic transformation of crop plants for herbicide resistance.
Resistance to specific herbicides has been shown to be the result of changes in enzymes which are involved in particular biosynthetic pathways. For example, the non-selective postemergence herbicide glyphosate acts by inhibiting the enzyme 5-enolpyruvyl-3-phosphoshikimate synthase (EPSP). Glyphosate tolerant plants have been produced by inserting into the genome of a plant the capacity to produce high levels of EPSP synthase and reference is made to U.S. Pat. No. 5,312,910. Also glyphosate tolerant plants have been produced by desensitizing EPSP synthase to glyphosate.
Acetolactate synthase (ALS) which catalyzes the first reaction in the biosynthetic pathway to the branched amino acids has been shown to be the site of action of several structurally unrelated classes of herbicides, including: sulfonylureas (LaRossa et al., J. Biol. Chem. (1984) 259:8753-8757), imidazolinones (Shaner et al., Plant Physiol. (1984) 76:545-546), triazolopyrimidines (Subramanian et al., ACS Sym. Series 389 (1989) pp 277-288) and pyrimidyloxybenzoates (EPA 223 406, EPA 249 707 and EPA 249 708). Other classes of herbicides with ALS as the target include pyrimidylsalicylates, carbamoylpyrazolines, sulfonylimino-triazinyl heteroazoles, N-protected valylanilides, sulfonylamide azines, pyrimidyl madelie acids, benzenesulfonyl carboxamide compounds, substituted sulfonyldiamides, and ubiquinone-o. Transgenic plants with decreased sensitivity to inhibition by sulfonylurea and imidazolinone herbicides have been disclosed. Particular mention is made of EPA 0 525 384; U.S. Pat. Nos. 4,761,373; 5,198,599 and 5,331,107 and references cited therein.
Since many of the ALS inhibitor herbicides are known for their low mammalian toxicity, high herbicidal potency at low use rates and broad range crop selectivity, crop hybrids or varieties with resistance to these herbicides would provide an attractive solution to allowing herbicidal use without risk of damage to sensitive crops.